In vitro antigen presenting cell-derived IL-10 and IL-6 correlate with Trichuris muris isolate-specific survival.
In vitro antigen presenting cell-derived IL-10 and IL-6 correlate with Trichuris muris isolate-specific survival.
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DOI：
10.1111/j.1365-3024.2008.01088.x
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发表时间：
2009-03
影响因子：
2.2
通讯作者：
Else KJ
中科院分区：
文献类型：
--
作者：
D'Elia R;Else KJ
Trichuris muris（小鼠鞭虫）被用作人类寄生虫 T. trichiura 的实验室模型。鼠毛虫存在三种实验室分离株——E、J 和 S 分离株。先前的数据表明，S 分离株在 C57BL/6 小鼠中长期存活，而 E 和 J 分离株则被驱逐。 S 分离株之所以能够持续存在，被认为是由于它分泌独特的排泄/分泌抗原，这些抗原与 APC 相互作用，从而不会产生保护性 T 细胞反应。为了确定 APC 对来自三个分离株的 E/S 抗原是否有不同的反应，我们在体外培养了分离株特异性 E/S 与骨髓源性巨噬细胞 (BMMΦ) 和树突状细胞 (BMDC)。通过 FACS 分析共刺激标记和 MHC-II 水平，并对上清液中的细胞因子水平进行定量。与 J 和 E 分离株 E/S 相比，S 分离株的 E/S 抗原持续刺激巨噬细胞 (F4/80+CD11b+CD11c−) 和树突状细胞 (CD11c+CD11b+F4/80−) 产生显着更高水平的 IL-10 和 IL-6。如果 APC 衍生细胞因子（特别是 IL-10）的这些体外差异在体内具有生物学意义，那么它们可能通过创建保护性免疫反应不太有效的调节性细胞因子环境来促进 S 分离株的存活。
Trichuris muris, the mouse whipworm, is used as a laboratory model of the human parasite T. trichiura. Three laboratory isolates of T. muris exist — the E, J and S isolates. Previous data have shown that the S isolate survives to chronicity in C57BL/6 mice unlike the E and J isolates, which are expelled. The ability of the S isolate to persist is thought to be due to it secreting unique excretory/secretory antigens, which interact with APCs such that protective T cell responses do not develop. To determine whether APCs respond differently to E/S antigens from the three isolates we cultured isolate-specific E/S with bone marrow-derived macrophages (BMMΦ) and dendritic cells (BMDCs) in vitro. Markers of co-stimulation and levels of MHC-II were analysed by FACS and cytokine levels in supernatants quantified. E/S antigens from the S isolate consistently stimulated significantly higher levels of IL-10 and IL-6 from both macrophages (F4/80+CD11b+CD11c−) and dendritic cells (CD11c+CD11b+F4/80−) compared to J and E isolate E/S. If these in vitro differences in APC-derived cytokines, particularly IL-10, are biologically significant in vivo, they may contribute to the S isolate survival, by creating a regulatory cytokine environment in which protective immune responses are less effective.
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影响因子：
5.4
作者：
KARASUYAMA, H;MELCHERS, F
通讯作者：
MELCHERS, F
影响因子：
1.6
作者：
Else, KJ;deSchoolmeester, ML
通讯作者：
deSchoolmeester, ML
影响因子：
6.4
作者：
Dissanayake, S;Khan, N;Lukic, M
通讯作者：
Lukic, M
DOI：
10.1111/j.1440-1681.2006.04400.x
发表时间：
2006-05-01
影响因子：
2.9
作者：
Harnett, W;Harnett, MM
通讯作者：
Harnett, MM
影响因子：
2.2
作者：
Lutz, MB;Kukutsch, N;Schuler, G
通讯作者：
Schuler, G